医学研究与教育
醫學研究與教育
의학연구여교육
MEDICAL RESEARCH AND EDUCATION
2015年
2期
6-10
,共5页
灯盏乙素%缺氧缺血%脑%p38 MAPK%凋亡
燈盞乙素%缺氧缺血%腦%p38 MAPK%凋亡
등잔을소%결양결혈%뇌%p38 MAPK%조망
scutellarin%hypoxia-ischemia%brain%p38 MAPK%apoptosis
目的:探讨灯盏乙素抗新生大鼠缺氧缺血性脑损伤的作用及对p38 MAPK表达的影响及机制。方法45只健康新生7日龄SD大鼠随机分为假手术组、缺血缺氧组、灯盏乙素组(25 mg/kg)。分别于用药后第24小时、3天、7天每组处死大鼠各5只,取脑组织切片。采用TUNEL染色检测神经细胞凋亡;采用免疫组织化学染色检测p38 MAPK的表达高峰、表达变化趋势。结果缺氧缺血后海马CA1区神经细胞凋亡,p38 MAPK表达增加;灯盏乙素组神经细胞凋亡及p38 MAPK表达均减少(与同一时间点缺氧缺血组比较差异有统计学意义P<0.05)。结论灯盏乙素可能是通过抑制p38 MAPK信号通路而减少神经细胞凋亡,从而发挥脑保护作用。
目的:探討燈盞乙素抗新生大鼠缺氧缺血性腦損傷的作用及對p38 MAPK錶達的影響及機製。方法45隻健康新生7日齡SD大鼠隨機分為假手術組、缺血缺氧組、燈盞乙素組(25 mg/kg)。分彆于用藥後第24小時、3天、7天每組處死大鼠各5隻,取腦組織切片。採用TUNEL染色檢測神經細胞凋亡;採用免疫組織化學染色檢測p38 MAPK的錶達高峰、錶達變化趨勢。結果缺氧缺血後海馬CA1區神經細胞凋亡,p38 MAPK錶達增加;燈盞乙素組神經細胞凋亡及p38 MAPK錶達均減少(與同一時間點缺氧缺血組比較差異有統計學意義P<0.05)。結論燈盞乙素可能是通過抑製p38 MAPK信號通路而減少神經細胞凋亡,從而髮揮腦保護作用。
목적:탐토등잔을소항신생대서결양결혈성뇌손상적작용급대p38 MAPK표체적영향급궤제。방법45지건강신생7일령SD대서수궤분위가수술조、결혈결양조、등잔을소조(25 mg/kg)。분별우용약후제24소시、3천、7천매조처사대서각5지,취뇌조직절편。채용TUNEL염색검측신경세포조망;채용면역조직화학염색검측p38 MAPK적표체고봉、표체변화추세。결과결양결혈후해마CA1구신경세포조망,p38 MAPK표체증가;등잔을소조신경세포조망급p38 MAPK표체균감소(여동일시간점결양결혈조비교차이유통계학의의P<0.05)。결론등잔을소가능시통과억제p38 MAPK신호통로이감소신경세포조망,종이발휘뇌보호작용。
Objective To study the effects of scutellarin treat HIBD in neonatal rats and the expression of p38 MAPK signal pathway following HIBD and its mechanism. Methods 45 healthy 7-day-old neonatal SD rats were randomly divided into sham operation group, HIBD group, and scutellarin group(25 mg/kg). After medication, each group respectively executed 5 rats in 24 h, 3 d, 7 d, and took brain tissue slice . The neuronal apoptosis was detected using TUNEL assay. The highest expression and expressional tendencies of p38 MAPK was determined by the method of immunohistochemistry. Results The apoptotic neurons, actived p38 MAPK increased after HIBD in the hippocampal CA1 region. The expression level of p38 MAPK and apopotic neurons in scultellarin group were signiifcantly lower than HIBD group (the differences of the same time point were statistically signiifcant P<0.05 ). Conclusion Scultellarin could reduce the apoptosis through inhibiting the p38 MAPK signal pathway with cerebral hemorrhage.